Friction reduction of animal joints is mediated by the superficial zone of the articular cartilage and by the lubricating ability of synovial fluid. Up until recently, no human diseases were clearly associated with a lack of chondroprotection by lubrication. Camptodactyly-arthroapthy-coxa vara-pericarditis (CACP) syndrome is an autosomal recessive pre-pubertal form of osteoarthrosis. The arthropathy is non-inflammatory in nature and appears histologically similar to osteoarthritis. This disease has been linked to a locus on chromosome 1q25 which expresses megakaryocyte stimulating factor (MSF; GenBank U70136). Expression of this gene also leads to both superficial zone protein expressed by chondrocytes and lubricin by synovial fibroblasts. Lubricin is a classical mucinous glycoprotein (5) providing boundary lubrication of apposed cartilaginous surfaces in the absence of viscosity. Lubricin is 50% (w/w) glycosylated with multiple residues of O-linked β(1-3)Gal-GalNAc which provides for lubricating activity (6). A CACP/lubricin knockout mouse was created that lacked the orthologous gene PRG4 for producing lubricin.
Presently, new investigational devices and drugs designed to improve or prevent arthritis are tested in animals with histological measures and in people with visual analog pain scales. There is presently no comprehensive joint function model with which to test molecules with a posited therapeutic benefit.